Abstract
Asthma is a very common disorder that still causes significant morbidity and mortality. A high percentage of individuals with asthma also experience exercise-induced bronchoconstriction (EIB). This article reviews the current literature and updates the reader on the safety, efficacy, and clinical applications of leukotriene modifiers in the treatment of EIB.
Highlights
Asthma affects 14 to 15 million people in the United States and is responsible for more than 100 million days of restricted activity, more than 5,000 deaths, and 470,000 hospitalizations each year.[1]
The liberated arachidonic acid is metabolized to various active compounds, including the leukotrienes LTB4, LTC4, LTD4, and LTE4 (Figure 1)
Subtype 1, CysLT1) on airway smooth muscle and bronchial vasculature, and they contribute to the bronchospasm, increased bronchial hyperresponsiveness, mucus production and mucosal edema, enhanced smooth-muscle cell proliferation, and eosinophilia that are characteristic of the asthmatic airway.[6]
Summary
Various biologic signals (including receptor activation, antigen-antibody interaction, and physical stimuli such as cold) activate cytosolic phospholipase A2 to liberate arachidonic acid from membrane phospholipids.[5]. Minute ventilation (exercise intensity), temperature and humidity of the inspired air (climatic conditions), and underlying baseline airway responsiveness are the primary determinants of the degree of EIB a patient will experience.[4] The exact mechanism leading to EIB is not yet fully understood but probably relates to drying and/or cooling of the airway mucosa and to mediator release.[3] Many studies, have demonstrated the protective effect of CysLT1 receptor antagonists against EIB, providing strong evidence of an important role of cysteinyl leukotrienes in regard to EIB.[10]
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